Aberrant regulation of bone trace elements in motheaten and osteopetrosis mutant mice.

G. Yamada, S. Nakamura, R. Haraguchi, M. Sakai, K. Suzuki, K. Miyado, Hidetoshi Hasuwa, Y. Ogino, T. Minami, Y. Tohno, M. Blum, L. D. Shultz

Research output: Contribution to journalArticle

1 Citation (Scopus)

Abstract

Increasing numbers of genetic diseases involving bone development and models for these diseases have been identified recently. Analysis of these bone diseases have revealed that regulated action of multiple growth factors and subsequent signal transduction are essential for normal bone formation. In this paper, two murine mutant mice viable motheaten and osteopetrosis are analyzed. Mice with the recessive 'viable motheaten' mutation express a severe immunodeficiency syndrome and bone defects. Mutations at the motheaten locus were shown to be the result of aberrant splicing of the gene encoding hematopoietic cell phosphatase (Hcph). Mice homozygous for the osteopetrosis mutation develop congenital osteopetrosis due to a severe deficiency of osteoclasts. It has been recognized that bone trace element composition analysis helps to define bone-related physiological conditions. We have analyzed bone trace element composition in viable motheaten and osteopetrosis mutant animal models in this study. In order to gain insights into the effects of particular genetic defects on bone trace element composition, inductively coupled plasma atomic emissions spectrometry (ICP-AES) analysis was performed. Marked changes in bone trace element levels were found in limb bones of viable motheaten and osteopetrosis mutant mice. An assessment of these trace element spectrum in the two mutant models with respect to each genetic defects are discussed in this paper.

Original languageEnglish
Pages (from-to)315-319
Number of pages5
JournalCellular and molecular biology (Noisy-le-Grand, France)
Volume44
Issue number2
Publication statusPublished - 1998 Mar
Externally publishedYes

Fingerprint

Osteopetrosis
Trace Elements
Bone
Bone and Bones
Mutation
Non-Receptor Type 6 Protein Tyrosine Phosphatase
Defects
Inborn Genetic Diseases
Bone Diseases
Bone Development
Osteoclasts
Chemical analysis
Osteogenesis
Signal transduction
Gene encoding
Signal Transduction
Spectrum Analysis
Intercellular Signaling Peptides and Proteins
Extremities
Animal Models

ASJC Scopus subject areas

  • Molecular Biology
  • Clinical Biochemistry
  • Cell Biology

Cite this

Yamada, G., Nakamura, S., Haraguchi, R., Sakai, M., Suzuki, K., Miyado, K., ... Shultz, L. D. (1998). Aberrant regulation of bone trace elements in motheaten and osteopetrosis mutant mice. Cellular and molecular biology (Noisy-le-Grand, France), 44(2), 315-319.

Aberrant regulation of bone trace elements in motheaten and osteopetrosis mutant mice. / Yamada, G.; Nakamura, S.; Haraguchi, R.; Sakai, M.; Suzuki, K.; Miyado, K.; Hasuwa, Hidetoshi; Ogino, Y.; Minami, T.; Tohno, Y.; Blum, M.; Shultz, L. D.

In: Cellular and molecular biology (Noisy-le-Grand, France), Vol. 44, No. 2, 03.1998, p. 315-319.

Research output: Contribution to journalArticle

Yamada, G, Nakamura, S, Haraguchi, R, Sakai, M, Suzuki, K, Miyado, K, Hasuwa, H, Ogino, Y, Minami, T, Tohno, Y, Blum, M & Shultz, LD 1998, 'Aberrant regulation of bone trace elements in motheaten and osteopetrosis mutant mice.', Cellular and molecular biology (Noisy-le-Grand, France), vol. 44, no. 2, pp. 315-319.
Yamada G, Nakamura S, Haraguchi R, Sakai M, Suzuki K, Miyado K et al. Aberrant regulation of bone trace elements in motheaten and osteopetrosis mutant mice. Cellular and molecular biology (Noisy-le-Grand, France). 1998 Mar;44(2):315-319.
Yamada, G. ; Nakamura, S. ; Haraguchi, R. ; Sakai, M. ; Suzuki, K. ; Miyado, K. ; Hasuwa, Hidetoshi ; Ogino, Y. ; Minami, T. ; Tohno, Y. ; Blum, M. ; Shultz, L. D. / Aberrant regulation of bone trace elements in motheaten and osteopetrosis mutant mice. In: Cellular and molecular biology (Noisy-le-Grand, France). 1998 ; Vol. 44, No. 2. pp. 315-319.
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